Abstract

Tumor necrosis factor-α (TNF-α) had been identified as a key pro-inflammatory cytokine in the pathophysiology of major depressive disorder (MDD) and the mechanism of antidepressant treatment. The primary aim of the present study was to examine the serum TNF-α levels in Chinese inpatients with MDD during the acute phase and to explore the changes in TNF-α levels after effective clinical treatment. Fifty-seven consecutive inpatients with MDD and 30 healthy controls were recruited. The serum TNF-α levels were detected using ELISA. Symptoms of depression were evaluated using the 24-item Hamilton Rating Scale for Depression (HAM-D-24). TNF-α levels and HAM-D-24 scores were assessed at baseline and after 2 and 12 weeks of follow-up. The serum TNF-α levels were higher in the MDD group than in the control group. After 2 and 12 weeks of antidepressant treatment, there were significant improvements in the patients' symptoms and significant decreases in the TNF-α levels. The baseline TNF-α levels significantly correlated with the decreased HAM-D-24 scores, particularly for the depressive symptoms of anxiety/somatization and weight loss. The present findings indicate that depression is accompanied by activation of TNF-α, which also has a predictive value for the antidepressant treatment response in patients with MDD.

Highlights

  • Major depressive disorder (MDD) has emerged as one of the most common psychiatric disorders [1]

  • The present study explored by setting up multiple follow-up points to examine the dynamic changes in the serum Tumor necrosis factor-α (TNF-α) levels in a fairly homogeneous group of major depressive disorder (MDD) patients treated with antidepressants in clinical settings

  • The primary aim of the current study was to examine the difference in the serum TNF-α levels in Chinese inpatients with MDD in the acute phase with healthy controls and, more importantly, to explore the changes in TNF-α levels and their predicting value for effective antidepressant treatment

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Summary

Introduction

Major depressive disorder (MDD) has emerged as one of the most common psychiatric disorders [1]. The inflammatory cytokine system is activated in several somatic diseases that share a number of common symptoms with MDD, such as tiredness. This implies that inflammatory cytokines may play a key role in the development of. Tumor Necrosis Factor-α Variations in Depression depression [3]. This theory well-explained some phenomena of psycho-neuroimmunological dysfunction in patients with MDD, who have an abnormal peripheral immune system [4]. It has been established that inflammatory cytokines can induce immune stimulation, which induces depression-like signs and symptoms, and these links have been supported by experimental and clinical evidences [5, 6]

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